Increased oxidative DNA damage in mammary tumor cells by continuous epidermal growth factor stimulation

J Natl Cancer Inst. 2001 Feb 7;93(3):214-9. doi: 10.1093/jnci/93.3.214.

Abstract

Background: Growth factors can enhance the malignant potential of tumor cells. To examine the relationship between growth factors and tumor progression, we previously established a weakly malignant cell line, ER-1. We found that a 24-hour exposure of ER-1 cells to epidermal growth factor (EGF) induced malignant properties (tumor progression) that were reversible but that, after a 1-month exposure, these changes were irreversible. In this study, we investigated the irreversible changes induced in ER-1 cells by a 1-month exposure to EGF and the possible involvement of oxidative stress.

Methods: ER-1 cells were treated with EGF (100 ng/mL) for 1 month in the presence or absence of an antioxidant, N-acetylcysteine or selenium, and compared with untreated control ER-1 cells. We assessed tumor progression by measuring intracellular peroxide levels, 8-hydroxydeoxyguanosine (a marker for oxidative DNA damage) levels, in vitro invasiveness, and in vivo tumorigenicity and metastatic ability. All statistical tests are two-sided.

Results: After ER-1 cells were treated for 1 month with EGF, levels of intracellular peroxide and 8-hydroxyguanosine in the DNA of treated cells were higher than those in the DNA of control cells, and treated ER-1 cells were more tumorigenic and metastatic in vivo and more invasive in vitro than untreated control cells (all P<.001). Levels of 8-hydroxyguanosine in DNA increased as the length of the EGF treatment increased (P<.001). However, when N-acetylcysteine or selenium was added with EGF for 1 month, levels of intracellular peroxide and 8-hydroxyguanosine in DNA were comparable to those in control cells (r =.795). Both tumorigenicity (P =.008) and metastatic ability (P<.001) decreased after addition of N-acetylcysteine or selenium.

Conclusion: The irreversible changes caused by continuous EGF stimulation of ER-1 cells result from increased oxidative damage in the DNA, which generates tumor cells with more malignant characteristics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 8-Hydroxy-2'-Deoxyguanosine
  • Acetylcysteine / pharmacology
  • Adenocarcinoma / drug therapy
  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism*
  • Animals
  • Antioxidants / pharmacology
  • DNA Damage* / drug effects
  • Deoxyguanosine / analogs & derivatives*
  • Deoxyguanosine / metabolism
  • Disease Progression
  • Epidermal Growth Factor / adverse effects*
  • Female
  • Free Radical Scavengers / pharmacology*
  • Glutathione Peroxidase / metabolism
  • Mammary Neoplasms, Experimental / drug therapy
  • Mammary Neoplasms, Experimental / genetics
  • Mammary Neoplasms, Experimental / metabolism*
  • Microscopy, Confocal
  • Oxidative Stress* / drug effects
  • Rats
  • Rats, Inbred SHR
  • Selenium / pharmacology
  • Tumor Cells, Cultured

Substances

  • Antioxidants
  • Free Radical Scavengers
  • Epidermal Growth Factor
  • 8-Hydroxy-2'-Deoxyguanosine
  • Glutathione Peroxidase
  • Deoxyguanosine
  • Selenium
  • Acetylcysteine